Atrial fibrillation is a cardiac arrhythmia that results in an irregular heartbeat. With atrial fibrillation, the normal electric impulses generated by the myocardium are overwhelmed by other electrical impulses in the heart. Atrial fibrillation includes the conduction of irregular impulses to the ventricles of the myocardium, which in turn generate the cardiac cycles of the heart and may result in disruption of the normal sinus rhythm of the heart. When left untreated, atrial fibrillation may become a chronic condition and lead to an increase in the risk of death.
Implantable medical devices (“IMDs”) may be implanted in a patient to monitor, among other things, electrical activity of a heart and to deliver appropriate electrical and/or drug therapy to treat atrial fibrillation, as required. IMDs include, for example, pacemakers, cardioverters, defibrillators, implantable cardioverter defibrillators (“ICD”), cardiac resynchronization therapy (“CRT”) devices, and the like. The electrical therapy produced by an IMD may include, for example, pacing pulses, cardioverting pulses, and/or defibrillator pulses to reverse arrhythmias (e.g., atrial and/or ventricular fibrillation, tachycardias, and bradycardias) or to stimulate the contraction of cardiac tissue (e.g., cardiac pacing) to return the heart to its normal sinus rhythm.
Known IMDs do not address some potential causes of atrial fibrillation. For example, one potential cause is atrial volume overload. Atrial volume overload represents the build up of fluid pressure in the left and/or right atria. As the pressure in the left and/or right atria increases, at least a portion of the myocardium stretches. Stretching of the myocardium in or near the atria may result in morphological and electrophysiological changes, which in turn may lead to the generation and maintenance of atrial fibrillation.
The body has a normal physiological mechanism to prevent atrial volume overload. This mechanism is referred to as the Bainbridge reflex, whereby an abnormally large amount of blood in the atria is sensed by stretch receptors in the atria. The stretch receptors signal the medulla of the brain to induce a reflex increase in the heart rate. Increasing the heart rate may increase the flow of fluid out of the atria in the heart and consequently reduce atrial pressure in the atria. As the atrial pressure is reduced, the atrial volume overload in the heart may be reduced. If the atrial volume overload can be reduced or prevented, especially in the early stages of pressure build-up in the atria, then the stretch-induced atrial fibrillation may be reduced or prevented. Moreover, even in patients with a long term history of coronary disease resulting in chronic atrial fibrillation, reducing atrial volume overload may result in the stretched myocardium in or near the atria reducing in size and thereby remodel. Atrial remodeling may, in turn, reduce the atrial fibrillation burden on the patient.
The potential exists that the Bainbridge reflex may either completely or partially fail in some patients, thus leaving these patients more susceptible to atrial volume overload and, consequently, atrial fibrillation. A need exists for a system and method that reduces atrial volume overload and thereby reduces the amount of stretch in the myocardium and consequently reduces or prevents the onset of stretch-induced atrial fibrillation.